Reasons Mental Deterioration Old Age Undiscovered Until 1906 Biology
Scientific articles quotes progressive deterioration about mental status in old age has been observed and briefed throughout the history. Until 1906, the exact reason of this mental deterioration was not clear.
In 1906, German physician, Dr.Alois Alzheimer's performed a brain autopsy in one of his patients died due to severe memory problems, confusion and difficulty in understanding questions. He noted highly dense aggregated structures around the nerve cells (neuritic plaques) and twisted bands of structures inside the nerve cells (neurofibrillary tangles). Hence the name of this degenerative disorder bears his name (Alzheimer's disease research association, 2010)
Scientific discovery of this degenerative disorder was founded out 100 years ago. During 1960s, scientists found out the relation between the decline in cognition and presence of plaques and neurofibrillary tangles in the brain. Scientists recognized this (Alzheimer's) as a disease and it is not a part of aging.
In 1990's the research on molecular level study of neuronal degeneration and susceptibility genes. Scientists worked on finding out genetic, environmental, and other risk factors responsible for the formation of amyloid plaques and neurofibrillary tangles.
FDA approved drugs were currently used to treat only the cognitive symptoms of the AD, and these drugs only slows the progressive decline in cognition.
Progressive changes in molecular environment of neurons and neurodegeneration has its implication in psychological functioning. Degenerative diseases are the diseases of grey matter characterized by the progressive loss of neurons which is associated with secondary changes in white matter of brain. The pattern of neuronal loss is selective, affecting one or more group of neurons leaving others intact. They arise without any clear inciting event in a patient without previous neurologic deficits.
The major critical degenerative diseases are Alzheimer's disease and Pick disease. Their clinical manifestation is seemed to be "dementia".
Dementia is the progressive loss of cognition independent of the state of attention resulting from diseases of the brain (Gilroy, 1985).It may be due to,
Therapeutic drug use (e.g. Atropine, Phenytoin,etc.,)
Metabolic systemic disorders (e.g. Acid-base disorders, hypo - ,hyperglycemia , haematological disorders ,Pulmonary insufficiency, Hypopituitarism, Cardiac dysfunction, Hepatolenticular degeneration)
Intracranial disorders(e.g. cerebrovascular insufficiency, chronic meningitis or encephalitis, neurosyphilis, HIV, Epilepsy,tumor,abscess,subdural hematomas, multiple sclerosis, normal pressure hydrocephalus)
Deficiency states (e.g. vitamin B 12 deficiency, folate deficiency, niacin or pellagra)
Collagen - vascular disorders : Systemic lupus erythematosus, temporal arteritis, sarcoidosis, Behcet's syndrome)
Exogenous intoxication: (e.g. Alcohol, Carbon monoxide, organophosphates, toluene, trichloroethylene , carbon disulfide, lead, mercury, arsenic, thallium, manganese)
Dementia is not part of normal aging and always represents a pathologic process. The present study investigates on the Alzheimer's disease where dementia is one of the clinical manifestations.
Alzheimer's disease - the most common form of dementia caused by progressive neuronal degeneration with pathological features showing the presence of amyloid plaques and neurofibrillary tangles, primarily affecting middle-aged and elderly individuals in whom it is cause of 70 percent of cases of dementia.(Perry et al.,2003)
The accurate etiology of Alzheimer's disease is unknown. The salient pathological features are the presence of amyloid plaques and neurofibrillary tangles. The "amyloid cascade hypothesis"(Hardy, 1991) is mainly investigated by the researchers and there is still the search for cause of Alzheimer's disease. The amyloid cascade hypothesis is supported by the study of early-onset Alzheimer's disease due to genetic factors. The mutation leads to increased formation of a particular form of a small protein fragment called A-Beta (AÎ²).The past and ongoing researches are focusing on the ways to slow down Alzheimer's disease is to decrease the amount of this protein in the brain, where it is one of the probable causative known.
SIGNS OF ALZHEIMER'S DISEASE:
Physicians keenly observe the following signs for complete evaluation
Loss of memory
Difficulty in familiar tasks performance.
Disorientation in time and place
Abstract thinking problem
Mood or behaviour changes
Loss of initiative.
In the first stages of Alzheimer's disease the memory problems initially observed as "normal part of aging" are. One of the common memory problems seen is short-term memory in early stage of Alzheimer's disease.
Personality changes like less spontaneity, lack of interest, and withdrawing from social interactions.
As the disease progresses:
Problems in intellectual functions develop.
Disturbances in behaviour and appearance.
Later in the course of the disorder:
Affected individuals may become confused or disoriented
Unable to define their place where they live or to name a place
Patients may wander
Unable to engage in conversation
Lose bladder and bowel control (Gilroy et al, 1995).
Final stages of the disease:
Death may follow due to pneumonia or problems of deteriorated conditions. Persons in their later age of life may be prone to die from other diseases (e.g. heart disease) rather than due to Alzheimer's disease.
TYPES OF ALZHEIMER'S DISEASE:
Early onset AD
Late onset AD
Early onset Alzheimer's: (EOAD)
It is a rare form of AD affecting the people before age 65. This type is seen in less than 10% of all AD patients. (Alzheimer's association, 2007) They experiences premature aging, so those people with Down syndrome are specifically at risk of this type. It is linked with a genetic defect on chromosome 14, where this is not the case in late onset AD. These chromosomal defects can undergo mutation of three genes namely presenilin1, presenilin2, and amyloid precursor protein (Selkoe, 2001). Myoclonus is one of the prevalent condition in AD seen in patients with early onset AD.
Persons with over the age of 65 may also prone to Alzheimer's. Late-onset Alzheimer's increases two folds for every 5 years after the age of sixty five. Though it is not hereditary and this sporadic Alzheimer's can affect any elderly person. On average people live roughly eight to ten years after diagnosis. Sometimes patients with sporadic Alzheimer are if they are associated with other diseases their life time reduces and lead to death.E4 type of gene is responsible for producing the apo lipoprotein. (Robin et al, 1999)
Familial Alzheimer's is entirely inherited. The affected families may show their inheritance to their off springs at least of two generations. It is rare, less than 1% of cases of Alzheimer's disease have FAD. Histological examination shows familial AD is indiscernible from other forms of AD. Amyloid protein forms plaques and neurofibrillary tangles that progress through the memory centers of the brain. The uniqueness of plaque is rare or uncharacteristic of AD. Due to mutation in one of the genes that generates abnormal protein with functional abilities, instead of the incapable gene products. Mutation in different genes like the amyloid precursor protein gene and the presenilin 1 and presenilin 2 genes have been discovered in patients with EOFAD (Selkoe, 2001). The products of these genes interact with the proteins in molecular level and involve in signal transduction between cells.
MANAGEMENT OF ALZHEIMER'S DISEASE:
The present management for the treatment of Alzheimer's is symptomatic. The acetylcholine esterase inhibitors were gaining importance in the management. Increasing the muscarinic function of the brain was clinical approach (Johnston, 1992).
The inhibition of AchE increases the Ach at the vicinity of neuronal Ach receptor.
Among the inhibitors physostigmine improved response in animal models of learning and causes mild transitory improvement in memory of patients with AD. Due to its short half -life and tendency of generating the symptoms of systemic cholinergic excess at therapeutic doses its use limited. Tacrine, donepzil, Rivastigmine, and Galantamine was approved by FDA in the treatment of AD (Mayeux, 1999).
Tacrine is one of the centrally acting AchE inhibitor (Freeman and Dawson, 1991). Oral Tacrine in combination with lecithin increases the memory performance (Chatellier and Lacombelz, 1990). Clinically tacrine is less in use because of its significant side effects like abdominal cramping, anorexia, nausea, vomiting, diarrhoea , elevation of serum transaminases and thus dose- limiting(Alzheimer's association, 2004).
Memantine, NMDA glutamate-receptor antagonist is an alternative in the management of AD.
The disease management of present scenario focuses on AchE inhibition and formation of new memories (Alzheimer's association, 2007). The existing Ach molecules are prevented from degradation and there by act on intact Ach receptors by the use of AchE inhibitors.
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